Non-invasive aortic impingement and core and cerebral temperature manipulation

ABSTRACT

A non-invasive method and apparatus for at least partially occluding the descending aorta of a patient and for manipulating core and cerebral temperature includes positioning an elongated tubular member which may have a moveable surface through the esophagus and displacing the moveable surface thereby applying a force posteriorly in the direction of the patient&#39;s descending aorta sufficient to partially or substantially completely occlude the descending aorta. The tubular member may include a heat exchange surface and a heat transfer mechanism for transferring heat to the heat transfer surface or for transferring heat from the heat transfer surface in order to modify the temperature of a portion of the patient.

CROSS-REFERENCE TO RELATED APPLICATION

This is a division of application Ser. No. 08/266,201, filed Jun. 27,1994, now U.S. Pat. No. 5,531,776.

BACKGROUND OF THE INVENTION

This invention relates generally to medical intervention and, moreparticularly, to the treating of cardiac arrest patients, patients invarious forms of shock, patients suffering hypothermia and hyperthermia,and patients with head injury. More particularly, this invention relatesto a method and apparatus for a non-invasive alteration of arterialblood pressures, myocardial and cerebral perfusion pressures, bloodflow, cardiac output, and cerebral and core temperatures.

Approximately one million people per year have cardiac arrests in theUnited States. Less than 10% of these people are discharged from thehospital alive without neurological damage. This percentage of peopledischarged would be increased if the treatment available after the onsetof cardiac arrest was improved. Areas in which this treatment could beimproved include: (1) artificial circulation during cardiopulmonaryresuscitation (CPR); (2) induction and maintenance of a state oftherapeutic hypothermia; (3) induction and maintenance of brief periodsof cerebral hypertension after return of spontaneous circulation; and(4) continued circulatory support for the brain and heart after returnof spontaneous circulation from cardiac arrest.

The blood of a cardiac arrest patient is artificially circulated duringCPR by cyclically compressing the chest. One major theory describing howartificial circulation is generated during CPR states that compressionof the chest causes global increases in intrathoracic pressure. Thisincrease in intrathoracic pressure in the thoracic compartment is evenlydistributed throughout the lungs, the four chambers of the heart as wellas the great vessels in the chest. The increase in thoracic pressure isgreater than in the compartments above and below the chest. Thesecompartments mainly include the neck and head above the chest and theabdominal compartment below the diaphragm and chest. When thoracicpressure is increased above the pressure in these compartments, bloodwithin the thoracic cavity moves to the head and abdomen with greaterblood flow going toward the head. When the chest is released, thepressure within the thoracic cavity drops and becomes less than thepressure within the head and abdomen, therefore allowing blood to returnto the thoracic cavity from the head and abdominal compartments. Thistheory of CPR-produced blood flow is termed the "thoracic pumpmechanism," whereby the entire thorax itself acts as a pump with theheart itself acting as a passive conduit for blood flow. This theory isdifferent from the cardiac pump mechanism, which states that compressionof the chest produces blood flow by compressing the heart between thesternum and anterior structures of the vertebral column. In mostpatients, blood flow produced during chest compressions is likely acombination of the two theories. In each individual patient, blood flowduring CPR depends on various factors such as body habitus, with thinnerindividuals relying more on the cardiac pump mechanism of blood flow,and in larger individuals with increased anterior-posterior chestdimension relying on the thoracic pump mechanism. Both mechanisms ofblood flow have been shown to be present in animal and human studies.Regardless of which mechanism is invoked, currently performed standardchest compressions as recommended by the American Heart Associationproduces 30% or less of the normal cardiac output. This results inextremely poor regional cerebral and myocardial blood flow during CPR.The level of blood flow generated during CPR is usually insufficient tore-start the heart and prevent neurologic damage. The purpose of CPR isto attempt to sustain the viability of the heart and brain until moredefinitive measures, such as electrical countershock andpharmacotherapy, are administered to the patient.

A main determinant for successful resuscitation from cardiac arrest isthe coronary perfusion pressure produced during CPR. Coronary perfusionpressure (CPP) is defined as the aortic diastolic pressure minus theright atrial diastolic pressure. CPP represents the driving force acrossthe myocardial tissue bed. Animal studies are plentiful whichdemonstrate that CPP is directly related to myocardial blood flow. Itappears in humans that a CPP of at least 15 mm Hg is required forsuccessful resuscitation. CPP of this magnitude is difficult to achievewith chest compressions alone. Patients, who utilize the thoracic pumpmechanism for CPR, are even more unlikely to be able to produce thislevel of CPP during CPR alone. The major means for producing coronaryperfusion pressures high enough for successful resuscitation have beento perform more forceful chest compressions and by administering variousadrenergic agonists, such as epinephrine. Unfortunately, it has beenshown that CPPs are difficult to augment with chest compressions aloneand that in some situations very high doses of adrenergic agonists arerequired to produce higher CPPs. The difficulty in trying to producehigher CPPs with CPR alone lies in the fact that right atrial diastolicpressures are sometimes increased to the same or greater magnitude asaortic diastolic pressures. Using various adrenergic agonists, aorticdiastolic pressure is usually augmented to a higher degree than rightatrial diastolic pressure. However, the use of adrenergic agonists toachieve this have several drawbacks. These include increasing myocardialoxygen demands to a greater degree than can be met with blood flowproduced during CPR. In addition, there are lingering effects ofadrenergic agonists which may be detrimental after successful return ofspontaneous circulation. These include periods of prolonged hypertensionand tachycardia, which may further damage the heart and possibly causere-arrest.

Cerebral perfusion pressure is a main determinant of cerebral bloodflow. During cardiac arrest and CPR, autoregulation of blood flow in thebrain may be lost. Cerebral perfusion pressure is defined as the meanarterial pressure minus the intracranial pressure. The main determinantof mean arterial pressure during CPR is aortic diastolic pressure. Oneof the main determinants of intracranial pressure during CPR is the meanvenous pressure in the central circulation and the neck. Forward flow tothe head is produced during CPR because of functional valves at the neckveins entering the thorax. These valves close during chest compressions,which prevent venous pressure transmission and flow of blood back intothe neck and cranium. When these valves are not functioning, pressure istransmitted during the chest compression to the neck veins and into thecranium. This in effect decreases forward cerebral blood flow. Methodsthat increase cerebral blood flow during conventional CPR are mainly theuse of adrenergic agonists. These agents selectively increase arterialpressure over venous pressure. Thus, mean arterial pressure becomesgreater than intracranial and cerebral venous pressure thus producingnet forward flow. However, use of adrenergic agonists have severaldrawbacks. In conventional doses, increases in cerebral blood flow areextremely variable with many individuals having no response at all. Theuse of higher doses of adrenergic agonists may be problematic aspreviously discussed under myocardial blood flow.

In summary, the major deficiencies in CPR-produced blood flow to thecritical organs of the heart and brain are primarily due to theinability of conventionally performed CPR to cause highly selectiveincreases in aortic diastolic pressure without causing increases ofsimilar magnitude in central venous pressures. The ability to maximizethe former while minimizing the latter would be extremely advantageousespecially if the effects could be immediately reversed.

Several techniques have been developed to take advantage of the variousCPR-produced mechanisms of blood flow. Two techniques that takeadvantage of the thoracic pump mechanism include simultaneousventilation compression CPR (SVC-CPR) and vest-CPR. SVC-CPR is atechnique that involves inflating the lungs simultaneously during thechest compression phase of CPR. This causes larger increases inintrathoracic pressure than external chest compression alone withoutventilation or without external chest compression. This has been shownin animal studies to result in higher cerebral blood flows than inconventionally performed CPR. However, one major drawback is thatcoronary perfusion pressures are not uniformly increased and, in someinstances, can be detrimentally decreased. When SVC-CPR was tested in aclinical trial, no increases in survival were noted over standard CPR.

Vest-CPR is a technique which utilizes a bladder containing vestanalogous to a large blood pressure cuff and is driven by a pneumaticsystem. The vest is placed around the thorax of the patient. Thepneumatic system forces compressed air into and out of the vest. Whenthe vest is inflated, a relatively uniform decrease in circumferentialdimensions of the thorax is produced which creates an increase inintrathoracic pressure. Clinically, the vest apparatus is cyclicallyinflated 60 times per minute with 100 mm Hg-250 mm Hg pressure which ismaintained for 30%-50% of each cycle with the other portion of the cycledeflating the vest to 10 mm Hg. Positive pressure ventilation isperformed independent of the apparatus after every fifth cycle. Whenstudied clinically in humans, and compared with manually performedstandard external CPR, the vest apparatus produced significantly highercoronary perfusion pressures and significantly higher mean aortic, peakaortic, and mean diastolic pressures. However, these changes are notuniformly seen in all patients. Of note, when the vest has been studiedin the laboratory and clinical settings, larger doses of epinephrinehave been used to achieve these higher coronary perfusion pressuressince the thoracic pump model would predict aortic diastolic and rightatrial diastolic pressures to be equivalent during the relaxation phase(when coronary perfusion occurs).

Another new technique, which takes some advantage of both the thoracicand cardiac pump mechanism of blood flow, is called "activecompression/decompression CPR (ACDC-CPR)." This technique utilizes aplunger-type device, which is placed on the patient's sternum duringcardiac arrest. The person performing chest compressions presses on thedevice which causes downward excursion of the anterior chest wall. Theperson then pulls up on the device. Since the device is attached to thesternum by suction, this causes the anterior chest to be activelyrecoiled instead of undergoing the usually passive recoil of standardexternal CPR. This active recoil is capable, in many individuals, ofcausing a decrease in intrathoracic pressure, which is transmitted tothe right atrium thus lowering right atrial pressure during artificialdiastole and, in turn, increasing coronary perfusion pressure. Thisnegative fight atrial pressure also has the effect of increasing venousreturn to the thoracic cavity, which may enhance cardiac output.Factors, such as body habitus and chest wall compliance, which impact onthe efficacy of ACDC-CPR have not been studied, but are likely to havean effect. Persons with larger body habitus probably would receive lessbenefit from the technique.

Two other techniques, which are being investigated to resuscitatevictims of cardiac arrest, and which do not rely on a mechanism ofCPR-produced blood flow, include selective aortic arch perfusion andcardiopulmonary bypass. Both of these techniques require access to thecentral arterial vasculature. Selective aortic perfusion is experimentaland involves percutaneously placing a balloon catheter in the aorticarch through a vessel, such as the femoral artery. The balloon catheteris placed in the aortic arch and the inflated balloon positioned justdistal to the take-off of the carotid arteries. Perfusion takes placeunder pressure with oxygenated fluids or blood for various lengths oftime. In this manner, the brain and heart are selectively perfused withlittle or no perfusion taking place distal to the occluded portion ofthe aorta. Over time, the central venous pressures will rise. Thistechnique has not been tested clinically, but is expected to take a highlevel of expertise and cannot be readily performed in a setting outsideof the hospital where many cardiac arrests occur.

Cardiopulmonary bypass during CPR is performed by obtaining centralarterial and venous access usually percutaneously through the femoralartery and vein. This technique is capable of totally supporting thecirculation by producing near normal cardiac outputs and blood flows tothe heart and brain. Although shown to be effective, there are manytechnical difficulties which make its widespread use unfeasible. Largecannulas must be placed in the femoral artery and vein, which isdifficult in the collapsed circulation. The bypass circuit iscomplicated and, if not properly primed, may produce air emboli. Inaddition, the patient requires systemic anticoagulation in mostinstances. The use of such a technique during CPR can be performed onlyat specially equipped centers with specially trained personnel.

Open-chest CPR is an old technique that was commonly performed beforethe advent of modern-day CPR. This technique involves opening thepatient's chest by performing a thoracotomy. The descending aorta isusually cross-clamped. The heart itself is then manually massaged(compressed) with the hands. Although this technique is effective inproducing heart and brain blood flows superior to standard CPR, it doesnot lend itself to widespread performance especially in theout-of-hospital setting. Reasons for this include the level of expertiserequired and the hazard of blood-borne pathogens. Other specialequipment, such as the Anstadt cup, can be directly placed on the heartto mechanically compress the heart but, of course, have the samedisadvantage of requiring a thoracotomy.

Two post-resuscitative interventions found to improve neurologic outcomein animal models of cardiac arrest is a brief period of immediatepost-resuscitation hypertension and rapid induction and maintenance ofcerebral hypothermia. The mechanisms for improved neurologic outcomewith post-resuscitation hypertension is unclear. It is thought that thisbrief period of hypertension clears cerebral vessels of microthrombi,which may clog the cerebral circulation following cardiac arrest. It isalso thought that this brief period of hypertension may help to preventsome of the post-resuscitation cerebral low flow "no flow phenomenon,"which contributes to neurologic injury. Post-resuscitation hypertensionmay decrease the overall amount of cerebral damage caused by cardiacarrest. One difficulty in providing for post-resuscitation hypertensionis that the common means of producing this, through the use ofadrenergic agonists, also produces considerable metabolic demands on thecardiovascular system.

Although shown to be very effective, production and maintenance ofpost-resuscitation hypothermia is extremely difficult to rapidly producewithin a time frame immediately after restoration of spontaneouscirculation following cardiac arrest. Although a decrease in cerebraltemperature from 37° C. to 34° C. has proven to be neuroprotective, evena small drop of 3° is difficult to rapidly produce. In order to beeffective, this mild degree of hypothermia must be produced withinseveral minutes of the resuscitation. Methods, such as isolated headcooling by placement of the head in an ice bath, nasopharyngeal cooling,injection of the carotid circulation with cooled solution, thoracic andperitoneal lavage, and placement of the head and thorax in a coolinghelmet and jacket are all problematic in that hypothermia is notattained rapidly enough or if attained cannot be maintained for asufficient duration of time to be neuroprotective. Althoughcardiopulmonary bypass can produce a state of therapeutic hypothermiavery rapidly, its institution either with traditional placement througha median sternotomy or through peripheral placement percutaneously viathe femoral artery and femoral vein is too time-consuming for it to beof practical use in the emergency setting. Thoracic and peritoneallavage, although effective, are also somewhat time-consuming andcumbersome in the emergency setting especially when ongoingresuscitative efforts are required. Carotid flush is effective but wouldinvolve needle or catheter placement into the internal carotid artery,which may be impractical, difficult to achieve, or unsafe. Althoughalmost immediate brain cooling can be achieved with carotid flushing,once restoration of spontaneous circulation is achieved, continuousinfusion would be required to maintain cerebral hypothermia. Coolingjackets and cooling helmets, along with placement of the head in an icebath, require too long of a time period to be effective in rapidlyreducing cerebral temperature. The main problem with these techniques isthat if cooling is not simultaneously accompanied by sufficient bloodflow, rapid temperature drops are unlikely to occur. This is especiallytrue of external cooling because the amount of blood flow andtemperature gradient required to cause rapid drops in core temperatureare quite large. The same problems exist when attempting to rapidlyinduce hypothermia in victims of head trauma.

Cardiogenic shock has many causes, including myocardial infarction,various forms of myocarditis, and other causes of myocardial injury.When severe, this condition becomes self-perpetuating secondary to theinability of the host to provide for adequate myocardial blood flow.This may result in further myocardial dysfunction leading to inadequatecerebral and myocardial blood flow and eventually to cardiac arrest.Cardiogenic shock may also be first noted after resuscitation fromcardiac arrest depending on the length of the cardiac arrest.Cardiogenic shock may sometimes be difficult to distinguish from otherforms of shock. Survival might be enhanced if myocardial and cerebralperfusion could be maintained until other definitive diagnostic andtherapeutic measures could take place.

Immediate survival from cardiogenic shock will depend on maintenance ofmyocardial and cerebral blood flow. Various forms of treatment areavailable for cardiogenic shock, including various forms ofpharmacotherapy and intra-aortic balloon pumping. Pharmacotherapy, whileeffective, requires invasive hemodynamic monitoring, such as pulmonaryartery catheter placement for optimal titration. This may be difficultto institute in a timely manner when severe cardiogenic shock is firstencountered especially in the pre-hospital setting. Intra-aortic balloonpumping in which a balloon catheter is placed into the thoracic aorta iseffective but somewhat complicated to perform. Special equipment isneeded for its placement and can only be performed at facilities whichare capable of placing and maintaining such equipment and patients.Intra-aortic balloon pumping increases cardiac output by decreasingcardiac afterload. A balloon inflates during the diastolic portion of acardiac cycle. This reduces cardiac afterload, thus lessening theworkload on the heart. This balloon inflation during diastole alsoforces blood cephalad, thus perfusing the myocardial and cerebraltissues more effectively.

Other forms of shock, such as septic and neurogenic shock, causehypoperfusion of critical organs due to a relative hypovolemia. Vasculartone is lost and requires a combination of volume replacement andvasopressors to maintain critical perfusion to vital organs. Immediateeffective therapy aimed at maintaining cerebral and myocardial perfusionis difficult to institute because the various forms of shock are attimes difficult to differentiate and therapy may differ between types ofshock, although the immediate goal is to preserve myocardial andcerebral perfusion.

The major underlying immediate cause of death from any shock state isinadequate myocardial and cerebral perfusion. Survival with intactneurologic function is likely to be enhanced if myocardial and cerebralblood flow can be maintained until the underlying cause of the shockstate can be optimally diagnosed and treated.

Head injury can be devastating. Much of the neurologic damage that takesplace occurs after the initial insult. Therapeutic measures, which havebeen shown to aid victims of head trauma, include induction oftherapeutic hypothermia and maintenance of cerebral blood flow in theface of increased intracranial pressure. These measures have beendifficult to institute within the first several hours after the initialinjury especially if other extra-cerebral organs are simultaneouslyinjured. Outcome might be improved in victims of head trauma ifmaintenance of cerebral blood flow with induction of mild hypothermiacould take place as soon after the initial injury as possible.

Hypothermia has been shown to improve the survival and reduce the amountof injured neurologic tissue. Several proposed mechanisms by which thishappens are decreases in the metabolic requirements of the injuredtissue, as well as decreases in the secretion of damagingneurotransmitters by the injured tissue. Production of hypothermia inhead-injured patients has been limited to cooling blankets, whichproduce whole body cooling. Although sometimes effective, whole bodycooling is difficult to initiate early especially in cases where otherorgan systems have been concomitantly traumatized in the initial injury.Blood flow to injured brain tissue is many times reduced below criticallevels required to maintain survival when intracranial pressure isincreased. Cerebral blood flow may be extremely difficult to maintainafter the initial injury especially when multiple organ systems areinvolved in the trauma. Mean arterial blood pressure can also bedifficult to maintain because of the ongoing blood loss into thethoracic and abdominal cavities or from extremity injuries. Intracranialpressure increases because of brain edema from the cerebral injury, orfrom expanding pools of blood from torn vessels in the brain or skullitself. Currently, the main mechanisms for reducing intracranialpressure involve the administration of diuretics, such as furosemide andmannitol, administration of steroids which reduce cerebral edema overtime, removal of cerebral spinal fluid, elevation of the head whichpromotes venous drainage, administration of barbiturates which reducethe metabolic demand of brain tissue, hyperventilation producinghypocapnia and reduced cerebral blood flow which decreases intracranialpressure, and, as a last resort, removal of less necessary parts of thebrain itself. Many of these therapies cannot be performed during theinitial care of the multiply injured trauma patient who has bothneurologic injury and multiple organ system injury, or have significantside effects. Administration of diuretics produce further volumedepletion and may further reduce mean arterial pressure. Steroidsrequire several hours to begin taking effect. Removal of cerebral spinalfluid and damaged brain tissue itself may take several hours to perform.Administration of barbiturates may also reduce the mean arterialpressure. Hyperventilation, although effective in reducing intracranialpressure, does so by decreasing cerebral blood flow which may beinjurious to damaged tissue. All of these therapies become morecomplicated in the presence of other extra-cerebral organ injury.Occasionally, pharmacotherapy to raise mean arterial blood pressure isused to help maintain cerebral perfusion pressure in the face of risingintracranial pressure. This is difficult and sometimes dangerous toinstitute early because vasopressors many times increase the metabolicdemands of other injured tissues.

Prolonged exposure to cold or hot environments under certain conditionscan result in life threatening states of hypo- or hyperthermia,respectively. Patients may be present with various forms of shock orvarious forms of altered mental status. Survival may be enhanced ifrapid normalization of body temperature (especially that of the heartand brain) takes place while maintaining adequate perfusion to the heartand brain. In cases of hypothermia, an attempt is made to raise corebody temperature as rapidly as possible to near normal levels. Lifethreatening dysrhythmias and dysfunction of the heart may simultaneouslyoccur from hypothermia, which makes ongoing rewarming efforts moredifficult to carry out. Methods of rewarming have included passiverewarming with blankets and heating lamps, and active rewarming withcardiopulmonary bypass, infusion of warmed intravenous fluids,peritoneal, bladder, gastric, thoracic, and mediastinal lavage, andbreathing of warm humidified air. Many of these methods are ineffectiveand are capable of only raising core temperature at a rate of 1° C. perhour. Some will be rendered totally ineffective based on the victim'scirculatory status. Others, such as peritoneal and thoracic lavage withwarm fluid, are effective but are time-consuming and difficult tocontrol. In addition, they cannot help support the circulation duringshock. Cardiopulmonary bypass is effective, but is time-consuming andrequires an extensive level of expertise. Most of these methods cannotbe performed outside of the hospital.

Treatment of hyperthermic emergencies requires the ability to rapidlylower the body's core temperature to normal in order to avoid shock,cardiac arrest, and various forms of neurologic damage. Treatmentscurrently used include ice packing, lavage of various body cavities withcooled fluids, and convection with water spray and fanning. Some of themethods will be totally ineffective based on the status of the patient'scirculation. In addition, if countershock or electrical cardiac pacingis required, safety hazards are present because the surface of the bodyis wet depending on the cooling technique used. In addition, none of theabove methods will be capable of simultaneously supporting thecirculation. Of course, the critical organs requiring support will bethe heart and brain.

Hemorrhagic shock is a leading cause of death from trauma. Many timesthere are delays in reaching hospitals which are qualified to take careof the complex injuries of such individuals. Many patients who die oftrauma, die from multi-system involvement. Multi-system involvement mayinclude head injury along with injuries to organs of the thoracic andabdominal cavity. Uncontrolled hemorrhage leading to hypovolemic shockis a leading cause of death from trauma especially from blunt andpenetrating trauma of the abdomen. When head trauma occurs concomitantlywith thoracic and abdominal hemorrhage, the brain becomes hypoperfusedand, thus, becomes at greater risk for secondary injury. Currently, inthe pre-hospital and emergency department setting, there are limitedmeans to control exsanguinating hemorrhage below the diaphragm whilemaintaining myocardial and cerebral blood flow. Definitive control ofhemorrhage is performed at surgery but this may be delayed and may notoccur within the golden hour (time from injury to definitivetreatment/repair) where the best opportunity lies in salvaging thepatient. Survival with improved neurologic outcome might be enhanced ifmeans were available to slow or stop ongoing hemorrhage (especiallybelow the diaphragm) while maintaining adequate perfusion to the heartand brain until definitive treatment of the hemorrhage is available.This would be especially true of trauma victims whose transport toappropriate medical facilities would be prolonged.

The use of the pneumatic anti-shock garment (PASG) has met with varyingdegrees of success depending on the location of injury. This garment isplaced on the legs and abdomen and is then inflated. Hemorrhage in theabdominal cavity, as well as the lower extremities, is controlledthrough tamponade while systemic blood pressure is raised partiallythrough autotransfusion and by raising peripheral vascular resistance.Use of the PASG can sometimes be cumbersome and does not uniformlycontrol hemorrhage or raise blood pressure. In addition, persons withconcomitant penetrating thoracic injuries may hemorrhage more when thedevice is applied. The device may also raise intracranial pressure,which might detrimentally alter cerebral blood flow resulting inneurologic injury.

Other more drastic means to control abdominal bleeding prior to surgeryhave been the use of thoracotomy to cross-clamp the thoracic aorta andthe use of balloon catheters placed into the aorta from the femoralarteries to a point above the celiac-aortic axis. These techniques havemet with varying degrees of success and require a high degree of skilland cannot be performed in hospitals not equipped to care for traumapatients or by paramedical care personnel.

Deliberately keeping hemorrhaging trauma victims in a hypotensive stateis currently being examined as a means to improve survival. This is donebased on the premise that overall hemorrhage (especially abdominalhemorrhage) is reduced if mean arterial pressure is kept low by notaggressively volume-repleting the victim prior to surgery.Unfortunately, this may be dangerous for trauma victims with concomitanthead injury or myocardial dysfunction.

An important cause of hemorrhagic shock not caused by trauma includesrupture of abdominal aortic aneurysms. These can occur suddenly andwithout warning. Control of bleeding even at surgery can be difficult.Temporary measures discussed above for hemorrhage secondary to traumahave been tried for hemorrhage secondary to aneurysm rupture. The samedifficulties apply. Survival might be enhanced if hemorrhage could becontrolled earlier while maintaining perfusion to the heart and brain.

SUMMARY OF THE INVENTION

The present invention provides a non-invasive method and apparatus fortreating cardiac arrest patients, patients in various forms of shock,such as hemorrhagic, cardiogenic, neurogenic and septic, patientssuffering hypothermia and hyperthermia, and patients with head injury.The invention relates to a device for inserting into an externallyaccessible tube of the patient, such as the patient's esophagus, toalter arterial blood pressures, myocardial and cerebral perfusionpressures, blood flow, cardiac output, and body temperatures of thepatient.

A non-invasive method of enhancing cerebral and myocardial perfusion ina patient, according to an aspect of the invention, includes positioninga device in a portion of the patient's esophagus juxtaposed with thepatient's descending thoracic aorta. The device is used to move, ordisplace, a wall of the portion of the esophagus posterior-laterally inthe direction of the descending thoracic aorta in order to at leastpartially occlude the descending thoracic aorta. This increases centraland intracranial arterial pressure without increasing central andintracranial venous pressure.

A non-invasive method of manipulating core and cerebral temperature of apatient, according to another aspect of the invention, includespositioning in the patient's esophagus a device having a heat transfersurface. The device is positioned in a manner that the heat transfersurface is juxtaposed with a thoracic vessel through which blood isflowing, such as the aortic arch, the carotid arteries, the descendingaorta or the heart. Heat is exchanged between the heat transfer surfaceand blood flowing through the vessel across the wall of the esophagusand the wall of the vessel.

A non-invasive device for at least partially occluding the descendingthoracic aorta of a patient and for manipulating core and cerebraltemperature of a patient, according to yet another aspect of theinvention, includes a tubular elongated member configured to a patient'sesophagus and having a selectively moveable portion. A displacementmechanism is included for selectively moving the moveable portion in amanner that will displace a wall of the esophagus that is juxtaposedwith the portion of the thoracic aorta of the patient in the directionof the aorta. In this manner, at least partial occlusion of thedescending thoracic aorta is effected. The device further includes aheat exchange mechanism for exchanging heat across the esophagus wallwith blood flowing through a thoracic vessel. In this manner, thebeneficial effects of the various aspects of the invention may becombined to provide a circulatory and temperature adjunct tocardiopulmonary cerebral resuscitation, hemorrhage, shock, head injury,hypothermia, and hyperthermia.

These and other objects, advantages, and features of this invention willbecome apparent upon review of the following specification inconjunction with the drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a side elevation of a device for at least partially occludingthe thoracic aorta of a patient, according to the invention;

FIG. 2 is the same view as FIG. 1 with a moveable portion and an anchorbladder of the device enlarged;

FIG. 3 is a sectional view taken along the lines III--III in FIG. 2;

FIG. 4 is a partial side elevation of an alternative embodiment of adevice for at least partially occluding the thoracic aorta of a patient,with portions removed to reveal internal structure;

FIG. 5 is a top plan view of the device in FIG. 4;

FIG. 6 is a sectional side elevation illustrating a human chest cavityand showing the preferred embodiment of the invention in an operativeposition;

FIG. 7 is a sectional view taken along the lines VII--VII in FIG. 6;

FIG. 8 is the same view as FIG. 6 with the moveable portion of thedevice enlarged in a manner to displace a wall of the esophagus in thedirection of the thoracic aorta;

FIG. 9 is a sectional view taken along the lines IX--IX in FIG. 8;

FIGS. 10a and 10b are side elevations of additional alternativeembodiments of a device for at least partially occluding the thoracicaorta of a patient, according to the invention;

FIG. 11 is a sectional view taken along the lines XI--XI in FIG. 10a;

FIG. 12 is a side elevation of a device for manipulating the core andcerebral temperature of a patient;

FIG. 13 is a side elevation of an alternative embodiment of a device formanipulating the core and cerebral temperature of a patient, accordingto the invention;

FIG. 14 is a device for at least partially occluding the thoracic aortaof a patient and for manipulating the core and cerebral temperature ofthe patient, according to the invention;

FIG. 15 is a sectional view taken along the lines XV--XV in FIG. 14;

FIG. 16 is a front elevation in section illustrating an apparatus forcounter-pulse pumping, according to the invention, in an operableposition;

FIG. 17 is a femoral artery pressure diagram of an experimental animalbleeding from the opposite femoral artery illustrating the resultachieved by the invention;

FIG. 18 is a carotid artery pressure diagram made concurrently with thediagram in FIG. 17; and

FIG. 19 is a carotid artery pressure diagram of an experimental animalillustrating operation of the invention after resuscitation from a20-minute cardiac arrest.

DESCRIPTION OF THE PREFERRED EMBODIMENT

Referring now specifically to the drawings, and the illustrativeembodiments depicted therein, in U.S. patent application Ser. No.08/126,542, filed by the present inventors on Sep. 24, 1993, for aMECHANICAL ADJUNCT TO CARDIOPULMONARY RESUSCITATION (CPR), AND ANELECTRICAL ADJUNCT TO DEFIBRILLATION COUNTERSHOCK, CARDIAC PACING, ANDCARDIAC MONITORING, now U.S. Pat. No. 5,626,618, the disclosure of whichis hereby incorporated by reference, an apparatus is disclosed thatincludes an esophageal bladder, which when inserted into the esophagusand expanded, hardens the esophagus to provide a platform posterior tothe heart against which the heart and aorta are compressed to provideimproved artificial circulation during CPR. The compression of the aortaincreases aortic pressure, which improves myocardial and cerebralperfusion. In order to further improve myocardial and cerebral perfusionpressure and blood flow, an apparatus 20 is provided for partially orcompletely occluding a portion of the thoracic aorta of a patient, suchas the descending aorta (FIGS. 1-3). Apparatus 20 includes an elongatedsemi-rigid tubular member 22, which is inserted into the esophaguseither nasally or orally. Tubular member 22 includes moveable portion24, which causes displacement of the esophagus posterior-laterallytowards the patient's left side, which allows a long segment of theesophagus to impinge upon an equally long parallel segment of the aortadistal to the aortic arch. Moveable portion 24 is illustrated in FIG. 1in its non-enlarged state. Apparatus 20 further includes a displacementmechanism 26 for displacing moveable portion 24 in order to displace theesophagus in a manner just described. In the embodiment illustrated inFIGS. 1 and 2, the moveable portion 24 includes a balloon 25, which isexpandable by a displacement mechanism 26, which includes connection toa source of pressure (not shown) through an esophageal lumen 28, whichextends to balloon 25 in order to enlarge the balloon. Apparatus 20 mayadditionally include a radial positioning device 30 attached to theportion of tubular member 22 extending outside the patient in order toallow radial adjustment of tube 22 to thereby position moveable portion24 in a manner that it will move posterior-laterally in the direction ofthe descending thoracic aorta. In the illustrated embodiment, radialpositioning device 30 is illustrated as a handle grip. Apparatus 20 mayfurther include a stomach bladder 32, which is radially offset frommember 22 and is enlargeable within the fundus of the stomach in orderto anchor member 22 in place. Stomach bladder 32 is enlargeable by astomach bladder lumen 34, which may be connected with a source ofpressure (not shown) in order to inflate bladder 32 after apparatus 20is positioned in the esophagus. Preferably, esophageal balloon 25 isinelastic so that it may be filled with a liquid or a gas and maintainedat a sufficient pressure so that it will be capable of impinging uponthe descending thoracic aorta sufficient to substantially completelyocclude the descending thoracic aorta. Preferably, esophageal balloon 25is expanded with an incompressible fluid, such as saline solution.

With apparatus 20 positioned in the patient's esophagus and expandableportion 24 expanded posterior-laterally in the direction of thedescending thoracic aorta, cerebral and myocardial perfusion pressuresare enhanced in much the same way as by cross-clamping the aortafollowing thoracotomy. This serves to cause an entirely selectiveincrease in central arterial systolic and diastolic pressure without anyconcomitant change in central venous and intracranial venous pressures.This, in turn, causes a non-pharmacological rapid increase in coronaryand cerebral perfusion pressures and, thus, myocardial and cerebralblood flow.

An alternative apparatus 20' for enhancing cerebral and myocardialperfusion includes a moveable portion 24' having a displacementmechanism 26', which includes a bow 36 made of spring steel and attachedat one end 38 within a tubular member 22' (FIGS. 4 and 5). A flexiblewire 40 extends through member 22' to the portion of apparatus 20'extending external to the patient (not shown). Wire 40 is attached to asecond end 42 of bow 36. In this manner, a tension force placed on wire40 external to the patient will contract the length of bow 36 resultingin the extension of bow 36 and, hence, displacement of moveable portion24'. Bow 36 is surrounded by a flexible sheath 44, which isolates thedisplacement mechanism 26' from the patient and allows expansion of thebow in the direction of the descending thoracic aorta of the patient.

In use, tubular member 22, 22' of apparatus 20, 20' is inserted in theesophagus 46 of the patient with optional stomach bladder 32 extendinginto the fundus of the stomach 48 (FIGS. 6-9). As best seen in FIG. 7,member 22, 22' causes the esophagus to become more circular in shape butdoes not impinge upon the descending aorta 50. Upon actuation ofdisplacement mechanism 26, 26', moveable portion 24, 24' is displacedposterior-laterally in the direction of descending thoracic aorta 50 inorder to impinge upon the aorta and partially, or substantiallycompletely, occludes the aorta, as best seen in FIGS. 8 and 9.

Although an apparatus for enhancing cerebral and myocardial perfusion,according to the previously described embodiments of the invention,includes a semi-rigid tube insertable into the patient's esophagus andhaving an expandable member which may be selectively expanded in thedirection of the descending aorta under the operation of a displacementmechanism, the invention may be practiced in other various forms. Anapparatus 20" includes a substantially rigid tubular member 22" having arigid permanently enlarged moveable portion 24" at an end opposite apositioning device 30 (FIGS. 10a and 11). In the illustrated embodiment,apparatus 20" is made of steel. Apparatus 20" may be nasally or orallyinserted into the esophagus and radial positioning device 30 manipulatedin order to position enlarged portion 24" in the direction of thedescending thoracic aorta in order to displace the wall of the esophagusand impinge upon the descending aorta.

An embodiment of a device for enhancing cerebral and myocardialperfusion, which does not require enlargement of the patient'sesophagus, is shown in FIG. 10b as an apparatus 20'" having a semi-rigidtubular member 22'" to which is pivotally attached a moveable member24'". Moveable member 24'" is pivoted in the direction of the patient'sdescending thoracic aorta by a displacement mechanism 26'" extendingthrough tubular member 22'" and operable externally or the patient. Whenapparatus 20'" is properly positioned in the patient's esophagus, thepivotal movement of moveable member 24'" displaces the esophagus wallinto impingement with the descending thoracic aorta in order topartially, or completely occlude the aorta, without substantiallyexpanding the esophagus wall.

Indeed, the invention may be carried out without the inclusion of radialpositioning device 30 provided that moveable portion 24, 24', 24", 24'"is properly positioned to displace the wall of the esophagus in thedirection of the descending thoracic aorta.

In addition to a steady-state, partial or substantially complete,occlusion, the present invention contemplates actuation of displacementmechanism 26, 26', 26'" in synchronism with the ventricular contractionsof the patient in order to provide a form of aortic counter-pulsepumping, thus simulating intra-aortic balloon pumping. By reference toFIG. 16, apparatus 20, 20', 20'" is inserted in the patient withdisplacement mechanism 26, 26', 26'" connected with an intermittentactuator 52. Intermittent actuator 52 is interconnected, as illustratedat 54, with an ECG monitor 56, which monitors the patient'selectrocardiogram by way of a pair of electrodes 58a, 58b to externallyor internally monitor the patient's electrocardiogram. Actuator 52actuates the displacement mechanism 26, 26', 26'" in synchronism withventricular diastole of the patient's cardiogram, as monitored by ECG56. The counter-pulsation mode, or counter-pulse pump, is most useful inenhancing perfusion pressure upon post-return of spontaneous circulation(ROSC) in order to counteract hypotension upon ROSC. In this manner,myocardial and cerebral blood flow is enhanced in this critical periodof ROSC. The counter-pulse pump is also useful in treating other formsof shock with myocardial dysfunction. Alternatively, actuator 52 may besynchronized with a pressure signal from a femoral, or upper extremity,arterial line instead of the signal derived from ECG 56.

When applying apparatus 20, 20', 20", 20'" to the patient, the degree ofocclusion of descending thoracic aorta 50 may be titrated to bloodpressure. This ensures that the apparatus is properly positioned. Suchproper positioning is critical for partial occlusion of the descendingaorta and counter-pulse pumping, as illustrated in FIG. 16. Bloodpressure may be advantageously monitored at the femoral artery,especially if the invention is used to treat shock states. If theapparatus 20, 20', 20", 20'" is utilized to treat ventricularfibrillation and/or cardiac arrest, then the degree of engagement may betitrated to the metabolic state of the myocardium. The ability tomonitor the metabolic state of the myocardium is disclosed in U.S. Pat.No. 5,077,667 issued to Charles G. Brown and Roger Dzwonczyk. Ifapparatus 20, 20', 20", 20'" is utilized to provide occlusion forinternal bleeding, then proper positioning is achieved when bloodpressure stabilizes.

An apparatus 60 is provided, according to the invention, formanipulating core and cerebral temperature of a patient (FIG. 12).Apparatus 60 includes a semi-rigid tubular member 62 for insertion inthe patient's esophagus and an optional stomach bladder 64 for anchoringmember 62 in the esophagus. Apparatus 60 further includes a heattransfer surface 66, which is positioned against the wall of theesophagus in the direction of a thoracic vessel through which bloodflows, such as the descending aorta. Heat transfer surface 66 extendssubstantially the length of the interface between the esophagus and thedescending aorta. Because there are less intervening tissues, such asskin, fat, cartilage, or bone, which may impede temperature change, heatmay be transferred more efficiently between the blood flowing throughthe descending aorta and heat transfer surface 66. Heat is supplied toor removed from heat transfer surface 66 by a fluid circulated throughtubes 68a, 68b, which extend between heat transfer surface 66 and a heatsource or heat sink 70. A stomach balloon lumen 72 provides for theselective inflation of a stomach bladder 64.

In operation, with apparatus 60 inserted in the esophagus of the patientsuch that heat transfer surface 66 is against the wall of the esophagusin the direction of the vessel, heat is either supplied to heat transfersurface 66 or withdrawn from heat transfer 66 by fluid flowing throughtubes 68a, 68b. The heat is, in turn, either removed from the fluid oradded to the fluid by heat source or sink 70. If it is desired to createhypothermia, heat source or sink 70 removes heat from the fluidcirculating through tubes 68a, 68b, which, in turn, cools heat transfersurface 66 which draws heat from the blood flowing through the vesseland cools the blood. This, in turn, lowers the core and cerebraltemperature of the patient. If it is desired to produce normothermia,heat is added to fluids flowing through tubes 68a, 68b from heat sourceor sink 70 which raises the temperature of heat transfer surface 66above the temperature of the blood flowing through the vessel. Thisraises the temperature of the blood flowing through the vessel and, inturn, raises the core and cerebral temperature of the patient.

An alternative apparatus 60' for manipulating core and cerebraltemperature of a patient includes a heat transfer surface 66' positionedwith respect to a tubular member 62' in order to abut the wall of theesophagus in the direction of a thoracic vessel through which bloodflows, such as the descending aorta. Apparatus 60' includes a secondheat transfer surface 74 positioned on member 62' in order to abut awall of the esophagus in a direction away from the vessel. Apparatus 60'further includes an electrically operated heat pump, such as athermoelectric device 76, which is capable of transferring heat betweenheat transfer surfaces 66' and 74. Such thermoelectric devices are wellknown in the art, are commercially available, and operate under thePeltier principle. Apparatus 60' includes a pair of electrical leads78a, 78b for connection of device 76 with an electrical source (notshown) in order to supply electrical energy to device 76. Depending uponthe polarity of the power supply, thermoelectric device 76 eitherremoves heat from heat transfer surface 66' and discharges the removedheat to heat transfer surface 74, or vice versa. The heat removed fromthe blood flowing through the thoracic vessel is discharged to thetissue surrounding the portion of the esophagus in contact with heattransfer surface 74. Likewise, heat added to the blood flowing throughthe thoracic vessel through transfer surface 66' is drawn from thetissue surrounding the portion of the esophagus contacted by heattransfer surface 74.

An apparatus 80 is capable of at least partially occluding thedescending aorta of the patient, as well as manipulating the core andcerebral temperature of a portion of a patient (FIGS. 14 and 15).Apparatus 80 includes a semi-rigid tubular member 82, which isconfigured for positioning in the esophagus of a patient. Apparatus 80may additionally include an optional radial positioning device (notshown) for manipulating the radial position of member 82 within thepatient's esophagus. Apparatus 80 further includes a moveable portion86, which is selectively displaceable in response to a displacementmechanism, such as a pressure applied to an esophageal lumen 92. In thismanner, with apparatus 80 properly positioned within the esophagus,moveable portion 86 will be capable of selectively displacing a wall ofthe esophagus posterior-laterally in the direction of a portion of thethoracic aorta, such as the descending aorta. Apparatus 80 furtherincludes a heat transfer surface 88 on moveable portion 86, whichengages a portion of the wall of the esophagus in the direction of thedescending aorta. A pair of tubes 90a, 90b circulate a fluid in thermalcontact with heat transfer surface 88 in order to transfer heat betweensurface 88 and a heat source or sink 70. Apparatus 80 may furtherinclude a stomach lumen 94 in order to selectively enlarge an anchoringstomach bladder 84. Tubular member 82 may be extruded of a semi-rigidpolymer with heat exchange tubes 90a and 90b, as well esophageal lumen92 and stomach lumen 94 formed therein, as illustrated in FIG. 15. Anoptional lumen 96 may be formed in tube 82 in order to provide forventing and/or suction of the stomach.

Apparatus 80 is capable of transferring heat to, or from, the bloodflowing through the descending aorta of the patient concurrently withpartial occlusion of the descending aorta in order to increase cerebraland myocardial perfusion. While apparatus 80 is also capable ofproducing substantially complete occlusion of the descending aorta, itis not expected that full occlusion would be useful in combination witha manipulation of the cerebral or core temperature, because the lack ofblood flow through the descending aorta would decrease the ability totransfer heat to or from the body.

Experimental verification of the efficacy of the invention may be seenby reference to FIGS. 17-19. In FIG. 17, a femoral artery pressuresignal taken from an animal who is allowed to bleed from the oppositefemoral artery illustrates the decrease in femoral artery pressure at Aconcurrently with initiation of bleeding in the animal. The apparatuswas applied to the animal at A in order to cause substantially completeocclusion of the descending thoracic aorta. FIG. 18 illustrates theincrease in carotid arterial pressure, beginning at point A,concurrently with the decrease in femoral arterial pressure of theanimal. This indicates that the hemorrhage is controlled whilepreserving or increasing myocardial and cerebral perfusion. The decreasein carotid artery pressure upon disengagement of the apparatus is seenat point B. FIG. 19 illustrates the effect on cerebral and myocardialperfusion during a cardiac arrest. The apparatus is applied to theanimal at A' upon resuscitation and ROSC after a 20-minute cardiacarrest. After engaging, the carotid artery pressure increases from 80/50mm Hg to 120/70 mm Hg. The apparatus is disengaged at B' and the carotidarterial pressure drops back to previous levels. This illustrates thatcerebral and myocardial perfusion can be enhanced in thepost-resuscitative hypotensive subject and that the effect can beimmediately reversed.

During cardiopulmonary resuscitation (CPR), an apparatus 20, 20', 20",20'" is inserted orally or nasally into the esophagus. The optionalstomach bladder is inflated and the displacement mechanism is operatedin order to cause maximum impingement of the descending aorta near itsbeginning. This serves to cause an entirely selective increase in aorticsystolic and aortic diastolic pressure without any concomitant change incentral venous or intracranial venous pressures. This, in turn, causes anon-pharmacologic rapid increase in coronary and cerebral perfusionpressure and, thus, myocardial and cerebral blood flow. Simultaneouswith this increase in perfusion pressure, the core and cerebraltemperatures may be lowered with apparatus 80 by circulating coolingfluid through the tubes extending to the heat transfer surface. Oncereturn of spontaneous circulation occurs, selective cerebralhyperperfusion, via selective hypertension, can be maintained for adetermined length of time if desired to help prevent post-resuscitationcerebral hypoperfusion. Depending on the state of the myocardium at thetime of return of spontaneous circulation (ROSC), the moveable portionmay partially impinge the descending aorta to various degrees, allowingpartial return of flow through the descending aorta. The apparatus maybe synchronized with ventricular contractions, as illustrated in FIG.16, in order to provide a counter-pulse pump during ventricular diastolein order to simulate intra-aortic balloon pumping. In states ofcardiogenic shock, as occur with myocardial infarction, post-cardiacarrest states, various forms of myocarditis, and other forms ofmyocardial injury, apparatus 20, 20', 20", 20'", 80 may be placed andengaged to cause immediate increase in myocardial and cerebral perfusionto prevent or reverse an agonal state. The moveable portion of theapparatus may be displaced intermittently or during ventriculardiastole, as synchronized with the electrocardiogram, to providecounter-pulse pumping. Apparatus 20, 20', 20", 20'", 80 can also be usedin the same manner in septic and neurogenic shock as a way toimmediately preserve or enhance myocardial and cerebral blood flow untilother definitive therapies can be carried out.

Patients with isolated head injuries or head injuries with concomitantextra-cerebral organ system injury may be treated by inserting apparatus20, 20', 20", 20'", 80 and by displacing the moveable portion to causevarious degrees of aortic impingement, thus causing preferentialincrease in mean arterial pressure to promote greater myocardial andcerebral blood flow. In addition, if therapeutic hypothermia is thoughtto be beneficial in a particular case, a cold fluid may be circulatedthrough tubes 90a, 90b to the heat transfer surface 88 to reducecerebral temperatures using apparatus 80. Such application may beparticularly helpful in head injury when other organs are injured, suchas those in the abdomen in which aortic impingement would reducehemorrhage while maintaining blood flow to the critically injured brain.While not reducing intracranial pressure, cerebral perfusion pressure ismaintained or increased by diverting flow proximal from the point ofaortic impingement until other definitive means of reducing intracranialpressure and maintaining cerebral blood flow can be instituted.

Patients with various forms of temperature extremes, such as hypothermiaor hyperthermia, may be rapidly brought to states of normothermia byplacement of apparatus 60, 60', 80 in the esophagus and transfer of heatto or from the blood flowing through the descending thoracic aorta inorder to change the core temperature appropriately. If the patientconcomitantly is in the state of shock, moveable portion 86 of apparatus80 may be displaced to cause various degrees of aortic impingement topreserve myocardial and cerebral blood flow until the state of shock canmore definitively be corrected.

Patients who are victims of trauma who do not respond to initialtherapies of oxygenation and volume loading, may have apparatus 20, 20',20", 20'", 80 placed into the esophagus orally or nasally. For victimsof trauma who are thought to be hemorrhaging into the abdominalcompartment or pelvis, the moveable portion may be extended to causecomplete occlusion of the descending thoracic aorta. This, in turn,would reduce the amount of blood flow to the injured compartment, thusreducing blood loss. At the same time, myocardial and cerebral perfusionare maintained or increased. The moveable portion is displaced untilformal control of hemorrhage can be obtained at operation or untilsufficient volume replacement has taken place. If the patient ishypothermic, warm fluid may be circulated through tubes 90a, 90b ofapparatus 80 to increase the patient's core body temperature. Themoveable portion may be intermittently retracted if blood flow to thespinal cord is thought to be compromised.

Thus, it is seen that the present invention comprehends a non-invasivetechnique for occluding the descending aorta and manipulating cerebraland core temperatures by transferring heat to or from blood flowingthrough the descending aorta and other thoracic vessels and heart. Theinvention is based upon the realization that the majority of thepopulation has the same relationship of the esophagus to the descendingthoracic aorta. The present invention has the ability to cause immediateincrease in aortic diastolic pressure in the aortic arch withoutincreasing venous pressure. This, in turn, causes an immediate increasein myocardial and cerebral perfusion. The present invention provides aneffect which is immediately reversible. The invention is useful duringhemorrhagic shock for its ability to decrease blood loss. The inventionis capable of extending the critical time from injury to definitivetreatment because it is readily useable by emergency care workers in thefield prior to, and during, transport of the patient to appropriatemedical facilities. The invention may be used by itself or incombination with other interventions, such as mechanical cardiopulmonaryresuscitation (CPR).

The invention effectively causes cerebral hypertension upon return ofspontaneous circulation (ROSC), thus helping to reduce the no-reflow andhypoperfusion phenomena, by perhaps preventing sludging in the cerebralmicrocirculation. The invention further effectively maintains myocardialand cerebral perfusion in the unstable ROSC state until more definitivemonitoring and therapy can be instituted. The invention may provide acounter-pulse pump, during a counter-pulsation mode, which impinges thedescending thoracic aorta to a varying degree in order to maintainoptimal post-ROSC myocardial and cerebral blood flow.

The invention is useful to produce and maintain a state of therapeutichypothermia to improve neurological outcome. Such states of hypothermiamay be readily reversed by the device, if necessary. The invention mayproduce normalization of body temperature from extremes of hypothermiaor hyperthermia while supporting myocardial and cerebral perfusionpressure and flow by various degrees of aortic impingement.

During the treatment of cardiogenic, septic, or neurogenic shock, theinvention provides for a counter-pulsation mode or various steady-statesof aortic impingement to optimize myocardial and cerebral blood flow toprevent cardiac arrest or cerebral damage until more definitive means oftreatment are instituted. The invention further provides for theoptimization of core temperature during treatment, if indicated.

The invention allows for the treatment of head injury by providingvarious degrees of aortic impingement, to redistribute and optimizecerebral blood flow in the face of mounting increases in intracranialpressure, or blood loss from extra-cerebral organ injury. Therapeuticcerebral hypothermia may be instituted, if needed.

In instances of exsanguinating hemorrhagic shock from various causes(trauma, aneurysms and the like) especially below the diaphragm, anapparatus, according to the invention, may be engaged to greatly reduceor stop blood pressure and blood flow below the point of aorticimpingement in order to reduce the amount of blood loss. While reducingthe amount of blood loss from injuries distal to the point ofimpingement, myocardial and cerebral perfusion pressure and flow ismaintained or enhanced. Impingement can be sequentially reduced tovarious degrees to allow judgment as to the effectiveness of ongoingvolume replacement effort or other efforts to control hemorrhage. Coreand cerebral temperatures may be manipulated, according to theinvention, to optimize therapy.

Changes and modifications in the specifically described embodiments canbe carried out without departing from the principles of the invention.In addition to the fluid and mechanical actuators disclosed herein,other forms of actuation, such as electrical and micro-mechanicalactuators, may be utilized. Furthermore, heat may be transferred toblood flowing through other thoracic vessels, such as through thepatient's heart, carotid arteries and aortic arch. The protectionafforded the invention is intended to be limited only by the scope ofthe appended claims, as interpreted according to the principles ofpatent law, including the doctrine of equivalents.

The embodiments of the invention in which an exclusive property orprivilege is claimed are defined as follows:
 1. A non-invasive devicefor at least partially occluding the descending thoracic aorta of apatient and for manipulating core and cerebral temperature of a portionof a patient, comprising:an elongated tubular member configured at leastin part to a patient's esophagus and having a selectively moveableportion at a juxtaposition with the patient's descending thoracic aorta;a displacement mechanism for displacing said moveable portion in thedirection of the patient's descending thoracic aorta when said tubularmember is positioned in the patient's esophagus; a heat exchange surfaceof said tubular member; and a heat transfer mechanism for transferringheat to said heat transfer surface or for transferring heat from saidheat transfer surface, said heat transfer mechanism transferring asufficient amount of heat to substantially modify the temperature of aportion of the patient.
 2. The device in claim 1 further including apositioning device for radially positioning said moveable portion in thepatient's esophagus.
 3. The device in claim 1 wherein said moveableportion is moveable sufficiently to cause substantially completeocclusion of said descending aorta.
 4. The device in claim 1 whereinsaid moveable portion includes a bladder and said displacement mechanismincludes a fluid lumen extending along said tubular member to saidmoveable portion for supplying fluid to enlarge said bladder.
 5. Thedevice in claim 1 wherein said moveable portion includes a mechanicalbow and said displacement mechanism includes a wire extending along saidtubular member in order to cause said bow to extend outwardly.
 6. Thedevice in claim 5 including a sheath covering said mechanical bow. 7.The device in claim 1 wherein said moveable portion includes a memberpivotally mounted to said tubular member and said displacement mechanismcauses said pivotally mounted member to pivot with respect to saidtubular member.
 8. The device in claim 1 including a heat source or heatsink for supplying heat to or extracting heat from said heat transfersurface.
 9. The device in claim 1 including an anchoring member foranchoring said tubular member in the patient's esophagus.
 10. The devicein claim 1 wherein said portion of the patient includes at least one ofthe patient's core and brain.
 11. A non-invasive device for at leastpartially occluding the descending thoracic aorta of a patient and formanipulating core and cerebral temperature of a portion of a patient,comprising:an elongated tubular member configured at least in part to apatient's esophagus and having a selectively moveable portion at ajuxtaposition with the patient's descending thoracic aorta; adisplacement mechanism for displacing said moveable portion in thedirection of the patient's descending thoracic aorta when said tubularmember is positioned in the patient's esophagus; a heat exchange surfaceof said tubular member; at least one of a heat source for supplying heatand a heat sink for extracting heat; and a heat transfer mechanism fortransferring heat to said heat transfer surface or for transferring heatfrom said heat transfer surface including a circulating fluid forexchanging heat between said heat transfer surface and said at least oneof a heat source and a heat sink.
 12. A non-invasive device for at leastpartially occluding the descending thoracic aorta of a patient and formanipulating core and cerebral temperature of a portion of a patient,comprising:an elongated tubular member configured at least in part to apatient's esophagus and having a selectively moveable portion at ajuxtaposition with the patient's descending thoracic aorta; adisplacement mechanism for displacing said moveable portion in thedirection of the patient's descending thoracic aorta when said tubularmember is positioned in the patient's esophagus; a heat exchange surfaceof said tubular member; and a heat transfer mechanism for transferringheat to said heat transfer surface or for transferring heat from saidheat transfer surface including another heat exchange surface of saidtubular member positioned away from said heat exchange surface and aheat pump positioned in said tubular member to pump heat between saidheat transfer surface and said another heat transfer surface.
 13. Thedevice in claim 12 wherein said heat pump includes a thermoelectricdevice.
 14. A non-invasive device for at least partially occluding thedescending thoracic aorta of a patient and for manipulating core andcerebral temperature of a portion of a patient, comprising:an elongatedtubular member configured at least in part to a patient's esophagus andhaving a selectively moveable portion at a juxtaposition with thepatient's descending thoracic aorta; a displacement mechanism fordisplacing said moveable portion in the direction of the patient'sdescending thoracic aorta when said tubular member is positioned in thepatient's esophagus; a heat exchange surface of said tubular member; aheat transfer mechanism for transferring heat to said heat transfersurface or for transferring heat from said heat transfer surface; and acontrol for said displacement mechanism that displaces said moveableportion in synchronism with the patient's ventricular contractions inorder to counter-pulse the patient's descending thoracic aorta duringventricular diastole.
 15. A non-invasive core and cerebral temperaturemanipulation device for placement within a human patient's esophagus,comprising:an elongated tubular member having a diameter substantiallyequal to the diameter of said patient's esophagus; a heat transfersurface on said tubular member located in a manner which abuts said heattransfer surface in heat transfer association against a wall of saidpatient's esophagus within which said tubular member is placed; and aheat transfer mechanism for transferring heat to said heat transfersurface or for transferring heat from said heat transfer surface, saidheat transfer mechanism transferring a sufficient amount of heat tosubstantially modify the temperature of a portion of the patient. 16.The device in claim 15 further including a positioning device forradially positioning said heat exchange surface in a patient'sesophagus.
 17. The device in claim 15 wherein said portion of thepatient includes at least one of the patient's core and brain.
 18. Anon-invasive core and cerebral temperature manipulation device,comprising:an elongated tubular member configured to fit at least inpart within a patient's esophagus; a heat transfer surface on saidtubular member; and a heat transfer mechanism for transferring heat tosaid heat transfer surface or for transferring heat from said heattransfer surface including another heat exchange surface on said tubularmember positioned away from said heat exchange surface and a heat pumppositioned in said tubular member to pump heat between said heattransfer surface and said another heat transfer surface.
 19. The devicein claim 18 wherein said heat pump includes a thermoelectric device. 20.A non-invasive core and cerebral temperature manipulation device,comprising:an elongated tubular member configured to fit at least inpart within a patient's esophagus; a heat transfer surface on saidtubular member; a heat transfer mechanism for transferring heat to saidheat transfer surface or for transferring heat from said heat transfersurface including at least one of a heat source and a heat sink externalof the patient and a circulating fluid for exchanging heat between saidheat transfer surface and said at least one of a heat source and a heatsink; and a positioning device for radially positioning said heattransfer surface in a patient's esophagus.
 21. The device in claim 20including a selectively moveable portion of said tubular member and adisplacement mechanism for selectively causing displacement of saidmoveable portion in the direction of the patient's descending thoracicaorta.
 22. The device in claim 21 in which said heat transfer surface ispositioned on said selectively moveable portion.
 23. A non-invasivedevice for at least partially occluding the descending thoracic aorta ofa patient, comprising:a tubular member configured at least in part to apatient's esophagus; a selectively moveable portion of the tubularmember positioned at a juxtaposition with the patient's descendingthoracic aorta when said tubular member is positioned in a patient'sesophagus, said portion moveable laterally a sufficient distance andhaving a surface of sufficient area to substantially completely occludethe patient's descending thoracic aorta; and a displacement mechanismfor displacing said moveable portion in the direction of the patient'sdescending thoracic aorta when said tubular member is positioned in thepatient's esophagus with a force sufficient to cause substantiallycomplete occlusion of the patient's descending thoracic aorta.
 24. Thedevice in claim 23 further including a positioning device for radiallypositioning said moveable portion in the patient's esophagus.
 25. Thedevice in claim 23 wherein said moveable portion includes a bladder andsaid displacement mechanism includes a fluid lumen extending along saidtubular member to said moveable portion for supplying fluid to enlargesaid bladder.
 26. The device in claim 23 wherein said moveable portionincludes a mechanical bow and said displacement mechanism includes awire extending along said tubular member in order to cause said bow toextend outwardly.
 27. The device in claim 26 including a sheath coveringsaid mechanical bow.
 28. The device in claim 23 wherein said moveableportion includes a member pivotally mounted to said tubular member andsaid displacement mechanism causes said pivotally mounted member topivot with respect to said tubular member.
 29. The device in claim 23including an anchoring member positionable in the patient's stomach foranchoring said tubular member in the patient's esophagus.
 30. The devicein claim 29 wherein said anchoring member is a stomach bladder.
 31. Thedevice in claim 23 including an occlusion indicator which indicatesdegree of occlusion of the descending thoracic aorta of the patient. 32.The device in claim 31 wherein said occlusion indicator includes anapparatus for measuring blood pressure at a particular location on thepatient.
 33. The device in claim 32 wherein said particular location isthe femoral artery.
 34. A non-invasive device for at least partiallyoccluding the descending thoracic aorta of a patient, comprising:anelongated tubular member configured at least in part to a patient'sesophagus; a selectively moveable portion of the tubular memberpositioned at a juxtaposition with the patient's descending thoracicaorta when said tubular member is positioned in a patient's esophagus; adisplacement mechanism for displacing said moveable portion in thedirection of the patient's descending thoracic aorta when said tubularmember is positioned in the patient's esophagus; and a control for saiddisplacement mechanism that displaces said moveable portion insynchronism with the patient's ventricular contractions in order tocounter-pulse the patient's descending thoracic aorta during ventriculardiastole.